1887

Abstract

Uninfected diabetes-related foot ulcer (DFU) progression to diabetes-related foot infection (DFI) is a prevalent complication for patients with diabetes. DFI often progresses to osteomyelitis (DFI-OM). Active (growing) is the most common pathogen in these infections. There is relapse in 40–60 % of cases even when the initial treatment at the DFI stage apparently clears infection.

adopts the quasi-dormant Small Colony Variant (SCV) state during DFU and consequently infection, and when present in DFI cases also permits survival in non-diseased tissues as a reservoir to cause relapse.

. The aim of this study was to investigate the bacterial factors that facilitate persistent infections.

People with diabetes were recruited from two tertiary hospitals. Clinical and bacterial data was taken from 153 patients with diabetes (51 from a control group with no ulcer or infection) and samples taken from 102 patients with foot complications to identify bacterial species and their variant colony types, and then compare the bacterial composition in those with uninfected DFU, DFI and those with DFI-OM, of whom samples were taken both from wounds (DFI-OM/W) and bone (DFI-OM/B). Intracellular, extracellular and proximal ‘healthy’ bone were examined.

was identified as the most prevalent pathogen in diabetes-related foot pathologies (25 % of all samples). For patients where disease progressed from DFU to DFI-OM, was isolated as a diversity of colony types, with increasing numbers of SCVs present. Intracellular (bone) SCVs were found, and even within uninfected bone SCVs were present. Wounds of 24 % of patients with uninfected DFU contained active . All patients with a DFI with a wound but not bone infection had previously had isolated from an infection (including amputation), representing a relapse.

The presence of SCVs in recalcitrant pathologies highlights their importance in persistent infections through the colonization of reservoirs, such as bone. The survival of these cells in intracellular bone is an important clinical finding supporting data. Also, there seems to be a link between the genetics of found in deeper infections compared to those only found in DFU.

Funding
This study was supported by the:
  • SA Allied Health Research Seed Funding.
    • Principle Award Recipient: TomP. Walsh
  • Australian and New Zealand Society for Vascular Surgery
    • Principle Award Recipient: JosephDawson
  • This is an open-access article distributed under the terms of the Creative Commons Attribution License.
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2023-06-16
2024-05-02
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